Introduction

At any given time, between 0.5% and 1% of children and adolescents suffer from clinically significant obsessive compulsive disorder (OCD) (Flament et al., 1988). Among adults with OCD, one-third to one-half develop the disorder during childhood or adolescence (Rasmussen and Eisen, 1990). Although some children persevere in the face of OCD, the disorder typically disrupts academic, social and vocational functioning. Hence, besides reducing morbidity associated with paediatric OCD, improvements in treating the disorder early in life have the potential to reduce adult morbidity.

Over the past 15 years, cognitive behavioral therapy (CBT) has emerged as the initial treatment of choice for OCD across the lifespan (March et al., 1997). Unlike other psychotherapies that have been applied, usually unsuccessfully, to OCD (March and Leonard, 1996), there is a logically consistent and compelling relationship between CBT, the disorder and the specified outcome (Foa and Kozak, 1991). Despite expert consensus that CBT is by far the best psychosocial treatment, clinicians routinely complain that patients will not comply with behavioural treatments and parents routinely complain that clinicians are poorly trained in CBT. Coupled with the lack of CBT-trained clinicians, the result is that many if not most children and adolescents are denied access to effective CBT. This unfortunate situation may be avoidable, given an increased understanding regarding the implementation of CBT in children and adolescents with OCD.

Introduction

Progress in the neurobiology of childhood anxiety has recently focused on the effects of rearing and environment in the progression of anxiety states. Convergence of evidence from both child studies of stress and trauma (Pfefferbaum, 1997; Pynoos, Steinberg & Wrath, 1995) as well as primate rearing and deprivation studies (Coplan et al., 1996; Higley, Suomi & Linnoila, 1992) illustrate that the effects of stress in the genesis of anxiety disorder can be profound. Anxiety disorders are now viewed from a developmental perspective (Ollendick, 1998; Rosenberg & Keshavan, 1998) in which an individual's history of exposure to threat and that threat's developmental and cognitive context are interwoven with internal factors (e.g. genetic and neurophysiological) as keys to the individual's ‘stress-response system’. Later in this chapter, neuroanatomical and information processing models of panic and childhood obsessive–compulsive disorders (OCD) are discussed in their developmental context in order to shed light on both the development of anxiety disorder and its frequent association with comorbid conditions, such as attention-deficit hyper-activity disorder (ADHD), in child psychiatry. The implication is clear: anxiety disorders, now viewed across the life span (Ballenger, 1997; Lydiard & Brawman-Mintzer, 1997), require treatments that reflect both the developmental stage and context of anxiety disorder genesis and maintenance.

Our understanding of the neurobiology of anxiety has been propelled by new pharmacological therapeutic tools specific in their impact on certain central nervous system (CNS) receptors within the ‘stress-response system’.